首页> 美国卫生研究院文献>Microorganisms >The Differential Phosphorylation-Dependent Signaling and Glucose Immunometabolic Responses Induced during Infection by Salmonella Enteritidis and Salmonella Heidelberg in Chicken Macrophage-like cells
【2h】

The Differential Phosphorylation-Dependent Signaling and Glucose Immunometabolic Responses Induced during Infection by Salmonella Enteritidis and Salmonella Heidelberg in Chicken Macrophage-like cells

机译:在鸡巨噬细胞的沙门氏菌和沙门氏菌海德堡感染期间感染期间诱导的差分磷酸化依赖信和葡萄糖免疫响应

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

is a burden to the poultry, health, and food safety industries, resulting in illnesses, food contamination, and recalls. subspecies Enteritidis ( Enteritidis) is one of the most prevalent serotypes isolated from poultry. subspecies Heidelberg ( Heidelberg), which is becoming as prevalent as Enteritidis, is one of the five most isolated serotypes. Although Enteritidis and Heidelberg are almost genetically identical, they both are capable of inducing different immune and metabolic responses in host cells to successfully establish an infection. Therefore, using the kinome peptide array, we demonstrated that Enteritidis and Heidelberg infections induced differential phosphorylation of peptides on Rho proteins, caspases, toll-like receptors, and other proteins involved in metabolic- and immune-related signaling of HD11 chicken macrophages. Metabolic flux assays measuring extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) demonstrated that Enteritidis at 30 min postinfection (p.i.) increased glucose metabolism, while Heidelberg at 30 min p.i. decreased glucose metabolism. Enteritidis is more invasive than Heidelberg. These results show different immunometabolic responses of HD11 macrophages to Enteritidis and Heidelberg infections.
机译:是家禽,健康和食品安全行业的负担,导致疾病,食物污染和召回。亚种EnterItidis(Enteritidis)是从家禽中孤立的最普遍的血清型之一。亚种海德堡(海德堡)变得普遍存在肠炎,是五种最孤立的血清型之一。虽然Enteritidis和海德堡几乎是遗传上相同的,但它们都能够在宿主细胞中诱导不同的免疫和代谢反应,以成功地建立感染。因此,使用Kinome肽阵列,我们证明Enteritidis和Heidelberg感染诱导毒蛋白,胱天蛋白酶,Caspases,Toll样受体和其他蛋白质中参与HD11鸡巨噬细胞的代谢和免疫相关信号传导的蛋白质的差异磷酸化。代谢通量测定测量细胞外酸化速率(ECAR)和氧气消耗率(OCR)证明了30分钟的肠炎虫(P.I.)增加了葡萄糖代谢,而海德堡在30分钟的P.I。葡萄糖新陈代谢降低。 EnterItidis比海德堡更具侵入性。这些结果显示了HD11巨噬细胞对肠炎和海德堡感染的不同免疫响应。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号